ANGIOTENSIN HYPERTENSION

Citation
Eh. Blaine et al., ANGIOTENSIN HYPERTENSION, Clinical and experimental pharmacology and physiology, 25, 1998, pp. 16-20
Citations number
20
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
03051870
Volume
25
Year of publication
1998
Supplement
S
Pages
16 - 20
Database
ISI
SICI code
0305-1870(1998)25:<16:>2.0.ZU;2-0
Abstract
1. One of the most important issues in the field of hypertension resea rch centres on the therapeutic use of inhibitors of the renin-angioten sin system (RAS), Inhibitors of the RAS have potent anti-hypertensive effects, even in experimental models of hypertension and in human esse ntial hypertension, where the activity of the peripheral RAS is low or normal. 2. It is suggested here that determining the mechanisms by wh ich activation of the peripheral RAS produces hypertension will help u s determine the anti-hypertensive effects of these inhibitors in low/n ormal renin-angiotensin hypertension. 3. Three hypotheses describing t he hypertensive effects of angiotensin are discussed. The first hypoth esis involves the direct vasoconstrictor effects of angiotensin, The s econd hypothesis suggests that chronic angiotensin produces hypertensi on by increasing Na+ reabsorption leading to volume expansion and hype rtension. The final hypothesis suggests that, in angiotensin-induced h ypertension, the increased Na+ reabsorption is not associated with vol ume expansion but, rather, is associated with an increase in vascular tone resulting from an interaction between angiotensin and the nervous system. 4. It is also hypothesized that the interaction between angio tensin and the nervous system produces a differential activation of sy mpathetic outflow that spares the kidney.